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Originally published In Press as doi:10.1074/jbc.M200305200 on September 28, 2002

J. Biol. Chem., Vol. 277, Issue 50, 48009-48019, December 13, 2002
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Transitional Type 1 and 2 B Lymphocyte Subsets Are Differentially Responsive to Antigen Receptor Signaling*

James B. PetroDagger §, Rachel M. Gerstein§, John LoweDagger , Robert S. CarterDagger , Nicholas ShinnersDagger , and Wasif N. KhanDagger ||

From the Dagger  Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0146 and the  Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655-0002

Mature B-lymphocytes develop sequentially from transitional type 1 (T1) and type 2 (T2) precursors in the spleen. To elucidate the mechanisms that regulate the developmental fate of these distinct B cell subsets, we investigated their biochemical and biological responses following stimulation through the B-cell antigen receptor (BCR). As compared with the T1 subset, T2 cells are more responsive to BCR engagement, as evidenced by their robust induction of activation markers, expression of the prosurvival protein Bcl-xL, and enhanced proliferation. BCR stimulation of T2 cells leads to the appearance of B cells with mature phenotypic characteristics, whereas T1 cells die. All of these T2 responses are dependent on the BCR signal transducer Bruton's tyrosine kinase, which is dispensable for the T1 to T2 transition. Furthermore, the serine/threonine kinases ERK, p38 MAPK, and Akt are predominantly activated in T2 compared with T1 B cells following BCR cross-linking. We conclude that T1 and T2 B cells respond differentially to BCR engagement via the induction of stage-specific signaling pathways. In turn, these signaling pathways probably govern the development and selection processes that are critical for the formation of the mature B cell compartment.

* This work was supported in part by a Vanderbilt University Graduate Dissertation Enhancement Award (to J. B. P.); the Vanderbilt-Ingram Cancer Center, National Institutes of Health (NIH) Grant T32 HL69765-01, American Cancer Society Grants RSG TBE-102299 and IRG-IN-25-00-01, and NIH Grants RO1 AI50213-01 and 1 P01 HL68744-01 (to W. N. K.); NIH Grant R01 AI43534 (to R. M. G.); NIH/DERC Grants 5 P30 DK32520 (to University of Massachusetts Medical School) and T32 HL69715-01 (to Jacek Hawiger).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors contributed equally to this work.

|| To whom correspondence should be addressed: Dept. of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-0146. Tel.: 615-343-5632; Fax: 615-343-7392; E-mail: Wasif.khan@mcmail.vanderbilt.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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